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The outcome of T‐cell costimulation through intercellular adhesion molecule‐1 differs from costimulation through leucocyte function‐associated antigen‐1
Author(s) -
Kohlmeier Jacob E.,
Rumsey Lisa M.,
Chan Marcia A.,
Benedict Stephen H.
Publication year - 2003
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2003.01578.x
Subject(s) - cd28 , microbiology and biotechnology , t cell , cytotoxic t cell , antigen , biology , immunology , immune system , in vitro , biochemistry
Summary Optimal T‐cell activation requires both an antigen‐specific and a costimulatory signal. The outcome of T‐cell activation can be influenced by the nature of the costimulatory signal the T cell receives. We recently demonstrated the ability of stimulation through intercellular adhesion molecule‐1 (ICAM‐1), resident on the T‐cell surface, to provide a second signal for T‐cell activation, and have extended that work here to begin an examination of the functional outcome of this set of signals. Costimulation through ICAM‐1 resulted in a greater percentage of cells having undergone more than three divisions when compared to costimulation through leucocyte function‐associated antigen‐1 (LFA‐1). Costimulation through ICAM‐1 also had an effect similar to costimulation through CD28 in its ability to down‐regulate the cyclin dependent kinase inhibitor p27 kip1 . Costimulation through ICAM‐1 provided greater protection from apoptosis than costimulation through LFA‐1, especially in cells having divided more than three times. This was supported by the ability of costimulation through ICAM‐1 to up‐regulate the anti‐apoptotic protein Bcl‐2. Finally, costimulation through ICAM‐1 or CD28 produced a greater number of T cells with a memory phenotype than costimulation through LFA‐1.